Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Tox MOA exam > tox > Flashcards

tox Flashcards

1
Q

Uncoupled phophorylation—> blocks or decreases ATP.

increased o2 demand in an effort to produce ATP

oxygen demand is more than o2 supply

resulting in overheating, metabolic acidosis and dehydration–>animal is cooked in its own heat./juices

irritation of the eye, GIT and intact skin

decresased cellular energy may cause neurotoxic and other effects

high exposure–>–>CNS stim/seizures

A

pentachlorophenol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

unknown but predominantly is a GIT mucosa irritant

damage skeletal mm

hydrolysis=how its metabolised

A

phenoxyderivative of fatty acids aka: 2,4-D herbicides

aka : phenoxy acetic acid derivative

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

MOA:

_____ inhibits the TCA/citric acid cycle therefore resulting in lack of energy and decreased cellular respiration and tissue damage.

  • increase in blood ___ , anaerobic glycolysis, blood lactate will icnrease and systemic acidosis will occur, increse glc also d/t no tca (this is what uses glc and no use=accumulation of glc)
  • d/t inhibition of tca: increase in lactate, blood ___, BUN, K+, and P04-, PCV and transaminases

death=cardiac or respiratory failure

A

urea–>–>Ammonia (NH3)

toxicity d/t ammonia, not the urea itsef

answer=ammoniA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

urea–> less than what age will be more sensitive d/t rumen condition?

and what age is tolerant?

A

1 year

3-6 weeks d/t underdeverloped rumen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

T/F : preconditioned animals are adpated to npn: urea therefore will be more tolerant?

A

true

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what increases toxicity of urea? (5)

A
  1. dehydration or low water intake
    2 . fasting: increases concentration of urea in blood
  2. feeds rich in urea
  3. hepatic insufficiency
  4. diet low in energy and protein but high in fiber: MOST IMP!!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

T/F: urea is in the NH4 form and tehrefore not absorbed ?

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

urea: nonionized or ionized?
nh3=nonionized ionized?

how oes this affect absorption?

A

urea=ionized and nh3=noonionized–>nh3 absorbed and urea isnt itself therefore exaplins why nh3 is the toxic component of this disaes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is the best lab specimen? for urea

A
  1. rumen fluid
  2. vitreous fluid of eye
  3. feed and urea content
  4. blood chemistry

note: specimes=FROZEN IMMEDIATELY

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what kind of disease is urea?

acute or chronic?

A

acute!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

how do u tx urea toxicosis?

A
  1. RELIEVE BLOAT
  2. give icey water to reduce the rxn
  3. give vinegar and acetic acid 5% to make the env acidic
  4. rumenotomy: most effective bc u remove rumen contents incl: urea and ammonia
  5. sodium bicarb=use bc its quicker in its axn then the lactated ringers would be.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

whats the most effective treatment for urea toxicosis in cattle?

A

RUMENOTOMY: removes the contents within the rumen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

T/F: D+ is NOT hemorhagic with urea toxicosis?

A

TRUE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is the most common cause of dairy cattle in usa?

A

monensin-ionophore toxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is a anti-coccidial in cattle?

A

monensin: ionophore

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what toxin causes a reduction in bloat and reduction of rumen acidosis in ruminants? ie: INHIBITS RUMEN MICROFLORA

A

monensin-ionophore

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what spp are affected and in what manor with ionophore/monensin??
and what spp most sensitive?

A

horse=most sensitive=purpose or accident by adding it to their feed

cattle: over error calculation of monensin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

t/f: horse and cattle that ingest recommended levels of monensin is going to be poisoned?

A

FALSE: if they eat recommended levels=not poisoned!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

sensitivity of monensin spp?

A

horse»cow»poultry/turkey

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

what is the drug of choice when you have monensin that is ingested and amplification of drugs used to treat intracellular organisms? (mycoplasma)

A
  1. tetracycline for both large and small animal and poultry
  2. if 1 doesnt work then you use floroquinolones for small animals

2 . but large animals/poultry, you use: tiamulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

name the drugs that can be used to tx monensin/ionophore toxicity?

A
  1. tetracycline
  2. fluoroquinolone-small animal
  3. large animal-tiamulsin
    other
  4. chloramphenicol
  5. erhythromycin
  6. sulfonamides
  7. cardiac glycosides (DIGITALIS: you can use bc monensin and other ionophores are cardiotoxic, but be aware this can causea wrosening in the toxicity of monensin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

explain why monensin/ionophore toxicity is more toxic in horses?
3 reasons why

A

so, d/t the mannor in which monensin is metabolized by the P450 enzymes in the liver, you are going to get that they are rapidly metabolized by P-450 oxidative demethylation enzymes in the liver and equines lack this demethylation oxidative enzymes and so the most toxic spp is the horse. IN ADDITION, this monensin is excreted in bile and bc horse doesn’t have a gal bladder, you cant get the monensin out!! IN ADDITION, the horse absorb
100% of this monensin!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

MOA: disrupt transmembrane electrochemical gradients and the main target is mitochondria of highly energetic tissues: myocardium, skeletal mm and the kidney. itll hit all tissues but mainly high energetic tissues.

  • influx of a+ ionophore complex increaes intracellular Na and this is accompanied by increaseing intarcellular calcium–>but cells try to gt rid of calclium
  • so sequestering of calcium will lead to by mitochondria and ininhibition of mito and dddecrease ATP energy (mito is the main organelle when it comes to energy and so dmaage=no energy for the cells who need high energy)
  • increase cytoplasmic ca also change pH in cell causing damge
  • cell death d/t disruptig homeostatic mechanisms
  • also, catecholamine release results in oxidaton pdts and free radicals causing sarcolemmal membrane damage (ie: calcium will release catecholamines)
  • finally, disruption of ion concentrations in excitable cells will cause dysfxn
A

monensin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what CS do u see in

  1. horse
  2. cattle
  3. poultry
  4. dogs
A

horse: CARDIAC TOXICITY, tachyA, SUDDEN death (dramatic signs in horses);;ataxia, colic, depression, sweating, hyperventilation
cattle: more skeletall mm signs, shown more than horses

poultry: same
dog: same

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what type of disease is monensin?: chronic or acute?

A

acute

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what are ddx for cattle of monensin tox?

A

vit E/selenium def

or Coffee Senna =dx is going to have chocolate urine color

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what are the ddx for horse for monensin tox?

A

colic or blister beetle ingestion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

wha are the clin path findings for monensin?

  1. elevated ezymes
  2. pcv?
  3. ion changes?
A
  1. CK, AST, ALP, LDH
  2. decrease blood Ca, K
    no change in Na
  3. increase PCV
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

how to tx monensin tox?

3 and one speciifc to horses

A
  1. mineral oil can decrease irriation and keep things moving quicker
  2. FLUIDS d/t high PCV
  3. vit E and selenium: give but make sure to give before and not after ie: dont reverse existing damage but can prevent further damge in the furture if this monensin toxicity were to occur
  4. horse shouldnt be stressed/ridden for many months
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what animals are more susceptible to Na ion toxicosis?what animal isnt?

A

cow, pig, chickens

NOT DOGS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

moa :

  • restricted water intake will increase the amount that is within the blood/csf–>and high na in the brain will cause cerebral edema and then it also inhibits glycolysis tehrefore lacking energy for the transport of na out of the brain
  • in addn: Na in the brain is going to attract water –>–>EDEMA
A

Na ion toxicosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what are main CS seen with na tox?: most animals

chickens: ?

A

seizures!! and edema in brain

chickens: depression, ascites, collapse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is a histopath pathopneumonic finding in pigs of na deprevation toxicicty?

A

eosinophilic menginoencephalitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

inorganic arsenic source?

A
  • wood preservative
  • roach and ant bait
  • insecticide, herbicide, fungicide and rodenticides
  • milk from poisoned cows may be toxic to calves, humans
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

types of toxicity of the inorganic arsenic?

A

peracute
acute
subacute

NO CHRONIC

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

whats the most toxic version of the inorganic arsenic?whats its axn?

A

trivalent: arsenite
- it will bind to SH group on an enzyme and inhibit the axn of the enzyem therefore we need a chelator to break this bond

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what spp is most susceptible to inorganic arsenic toxicity?

A

herbivores

38
Q

inorganic arsenic is found highly concentrated in what tissues?

A

kidney and liver d/t the high blood flow to these areas.

39
Q

T/F : inorganic arsenic does not cross BBB

A

true

40
Q

how is inorganic arsenic excreted?

A

urine, rapidly within 24 hours

41
Q

MOA:

the trivalent ___:

binds to 2 SH groups of lipoic (thioctic acid) and the trivalent will inhibit the lipoic (thioctic) acid

inhibition of lipodic acid inhibtis/ slows down glycolysis==>lower energy , TCA, and oxidative enzymes

(places like the GIT has tons of oxidative enzymes therefore we know this is a more senstive area that is affected by this toxin) and in kidney!!! (endothelial cap cell =leak=edema=hemorhage)

pentavalent:
- uncouples oxPhos (no fever) and may interfere with vit B1 and B6 metabolism

outcome: local corrosive effect, it isnt only mechanical but its also d/t inhibition of the oxidative enzymes: lack energy and that damages the GI mucosa

in addn: ause hypovolemia and electrolyte imbalance–>shock and –>death

A

inorganic arsenic

42
Q

source of urea tox?

A
  1. salt licks
  2. drink water with salt
  3. ice melts: dog
  4. dog on beach drink water from sea
  5. over crowding
  6. frozen water
  7. unpalatable water
43
Q

signs of inorganic aresenic toxicity?

peracute: CS and time?

acute?: CS and time? :

A

peracute: sudden death d/t hypovolemic shock: sec-min
acute: rapid onset, colic, salivation, vomit, thrist, WATERY D+ which may be hemorhagic=mintes -hrs
subacute: D+ with blood/mucosal shreds, depression, anorexia, colic, etc. : hrs-days: less severe in the git, but also include paralysis of hind limbs

typical GI signs, anorexia, V+, hemorhagic D+, hypovolemia and can get corrosive perforation

44
Q

what is the MOST IMP ANTEMORTEM AND POSTMORTEM specimens to collect for inorganic arsenic?

A

AM: urine
PM: kidney and liver

see increase PCV, and increased BUN

45
Q

how do u tx inorganic arsenic poisoning?

A
  1. tx hypovolemia and shock: fluids and electrolytes
  2. tx acidosis
  3. activated charcoal
46
Q

what is contraindicated in the tx of inorganic arsenic poisoning?

A
  1. gastric lavage
  2. emetics and
    3 strong cathartics
    4 peptobismal aka: has salicylic acid in it
47
Q

what is chelation options for inorganic acid?: ie: what is the chelator of choice and which of the two chelators is going to be less harmful?

A

dimercaprol: BAL, british antilewisiste
- chelator of choice
- not 100% effective
- may increase toxicity by mobilization of aresenic (bind to metal)

dimercaptosuccinic acid: DMSA, succimer, chemet : less effective and less toxic bc less lipidsoluble
-causes peripheral neural toxicity

48
Q

moa of organic arsenic?

A

peripheral nn damage, axonal damage very simialr to animals with vitamin B deficiency

49
Q

list the CS of organic arsenic tox of pigs and chickens?

A

…nts

50
Q

what are common lesions of organic arsenic poisoning?

A

-peripheral nn and optic nn degeneration, gliodsis and demylination

51
Q

what are the ddx for an animal with subacute selenium toxicosis (paralysis w/o blindness) in pigs? or vitamin B deficiency

A

ARSANILIC ACID

52
Q

what is source of excess copper? aka : chronic Cu toxicicty

A
  1. feed additives: =GRAS: generally recognized as safe
  2. natural cu in soils and plants
  3. mining
  4. metals in soil and water and can get absorbed into plants and eating these plants lead to toxicosis
  5. IMP: crap of chickens and pigs=eaten by sheep=toxicosis

bc the chickens and pigs arent susceptible to tox by Cu

53
Q

whats the normal Cu to molybdenum ratio?

A

6:1

54
Q

how is Cu excreted?

A

URINE: its going to bind to molybdate (molybdenum form) and then binds and forms copper molybdate and this is excreted out urine

55
Q

accumulation of cu in the liver is d/t imbalanced ratio of what compounds?

A

imbalanced btwn cu, molybdenum and sulfate

56
Q

how is Cu excreted?

A

bile

57
Q

what is a factor that induces Cu to come out of liver and cause toxicosis to sheep?

A

STRESS

58
Q

what does stress do to sheep with Cu accumulated within the liver?

A

causes hemolysis –>hemolytic anemia

59
Q

moa of cu?

A

Cu in liver causes liver degeneration and necorsis. release from the liver by stress causes oxidation of RBC membranes and this increases fragility of membrane and therefore causes a hemolytic crisis bc its easily stressed out. in addn, Cu will oxidize the hb to methb-emia: CHOCOLATE BLOOD!!

60
Q

cs of Cu toxicosis?

A

-shock, pale mm, icterus, sudden weakness, anorexia, resp signs bc hb cant carry o2 d/t metjbemia

61
Q

what specimens do u collect from a sheep : Cu toxicosis, if alive or dead?

A

alive: serum and whole blood
dead: elevated liver enzymes: LIVER -AST and LDH
- kidney also

62
Q

what is the chelator of choice for Cu tox?

A

D-penicillamine: expensive for sheep and sometimes used in dogs

63
Q

whats the Cu difference in dogs from sheep?

A

it only causes liver necrosis and not hemolytic crisis

64
Q

how to tx / pv Cu toxicossi in sheep?

5

A
  1. D-penecillamine
  2. Supplemental Zn
  3. molybendum: ADD ASAP!! wont help if given later on
  4. ammonium tetrathiomolybate
  5. ammonium molybdate: given once per day
65
Q

EQ: ddx for Cu toxicosis?

A
  1. hemolytic agents: zinc, napthelene, DMSO, guaifenesin, phenolics,
  2. poisonous plants: onion, gossypol, red maple, mustard
  3. certain snake venoms
  4. infectious dz: lepto, babesia, anaplasmosis, bacillary hemoglobinuria
66
Q

what conditions favor Pb absorption?

A

acidic

67
Q

source of pb?

A

aeriel emmision from conbustion of pb fuel, battery waste, insecticide, herbicide, Pb based paints most common source of toxicosis in homes built before 1960s , pet toys, pet dish, ceramics, etc.

OCEANS!!

a thumbnail sized chip of pb based paint may contain 50-200 mg of Pb

68
Q

which is more toxic organic or inorganic Pb?

A

organic!! more readily absorbed

69
Q

which metal has an effect of plumbism? what is it?

A

Pb –> its one of te most common toxicoses of acute-chronic toxicities. its where you get the pb2+ repalceing the ca 2+ and ZINC 2+ in the body.

young»old patients d/t immature BBB and GIT absorption

dog»=DEATH of puppies

birds=avian plumbism, avian saturism
goat , pig, chicken=more resistant than dogs

70
Q

MOA:

interferes with the cel and can replace Ca, Zn, Mg, Fe 2+

competes in the bone with Ca and alters the movement of Ca across the membranes.

XBBB,PLACENTA, GIT (better absorbed in stomach: acidic env)

breakdown of BBB throguh toxic effect on the blood vessel endocthelim cells and alteration of microvascular systems will make the BV weak and induce leakage–>edema in that area

forms complexes SH

also binds to methallothioninE: this is a livEr enzyme that will be a chelating protein involved in cellular detox and bc this ___ is bound to it, we are then going to get that there will be sequestered pb ions that are elevated in concentration bc they are just sitting on it.

bound to rbc for 60-90% of the RBC and this will induce damage.

A

pb

71
Q

what are the cs of pb?
GIT
RBC
CNS

A

GIT: caustic, anorexia, salivate, vomit, Pb colic, rumenatomy

RBC: anemia, basophilic stippling*

cns: spontaneous release of gaba=block neuroTs =hyperstimulation and cns depression: increase gaba and ach and cause mixed effects: hyperstim: ach and gaba: depression of cns

72
Q

target tissues of toxicity of the pb?

A

cns, git,rbc

73
Q

what specimens do we check for AM and PM of pb?

A

AM: whole blood and
PM: kidney, liver and git

74
Q

most common pb chelator?

A
  1. calcium disodium edta
75
Q

sources of zinc?

A
  1. pennies (post 1982)
    2galvinized metals
  2. zinc oxide in shampoos and stuff
  3. OD on zinc supplementation
76
Q

which heavy metal undergoes enterohepatic recirculation?

A

ZINC

77
Q

how does zinc circulate?

A

*plasma proteins: albumin and globulins

78
Q

moa of zinc?

A
  1. unknown but most consistent is intravascular hemolysis–>hemolytic anemia and lead to hemoglobinuria and hemoglobinemia
  2. injury to RBC, liver, kidney, pancreas
  3. Zn mediated hemolysis
  4. zinc mediated kidney damge: secondary to hemolysis
79
Q

IMP: how is zinc excreted?

A
  1. liver is a major organ of excretion and metabolism..
    - metallothionein: sequester metal and excretes
    - glutathione: sequester free radicals and associated with zinc toxicity
80
Q

what are the CS of zinc?

A

acute, chronic, peracute

  1. GIT: caustic–>anorxia, v+, lethargic, d+, pica
  2. hematologic /rbc damage: hemolytic anemia, jaundice, etc.
  3. renal (cell damge): azotemia: elevated BUN, hyperP
81
Q

what to use for analysis of zinc?

A

royal/dark blue top–>trace element tubes

82
Q

chelating agent for zinc?

A

calcium di-sodium edta or d-penecillamine

  • note: chelation may increase absorption and distribution from the intesteins and cause further damage to kidneys
  • guarded to poor outcome if patient experience
83
Q

what are common routes of iron?

A

PO, IV

IV»IM»>PO=toxicity

IV: piglets!!!! most toxic

84
Q

state of iron and how are they transported?

A
  1. ferrous: 2+
  2. ferric : 3+

*hemosiderin, ferritin and transferrin =iron brinding protein that transport it

85
Q

how is iron toxic? ie: whats its use of changing states and how does that affect organs

A

Fe is very unstable in that it changes quite quickly from Fe2+ to Fe3+ and this will induce free radicals to be released (ROS, glutathione) and this will in turn–> cellular damage–>tissue death–>organ failure

86
Q

what is chelator of choice for Fe?

A

deferoxamine (desferal)

87
Q

CS of Fe, that is unique? and general organs affected?

A
  1. GIT
  2. heart
  3. liver

*unique=follows 4 stages of toxicity

88
Q

acute toxicosis of Fe will bind to which protein? but in general for TK binds to which one?

A

ferretin

transferrin

89
Q

moa:
involved in copper deficiency!!!
-Cu involved in hematopoiesis, CT metabolism, myelin formation, pigmentation, none

Cu imp for absorption of Fe and tehrefore you get microcytic anemia(iie: Fe deficiency anemia)

in addn: Cu imp for cytochrome oxidase and metabolizing enzymes

in addn: copper containing prt in most aerobic cells have superoxide dismutase activity

A

Molybdenum

90
Q

best specimen : whole bloood for molybdenum: T/F

A

True

Tox MOA exam (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions